ArticleJournal of cellular and molecular medicine2024
USP22 Promotes Osteosarcoma Progression by Stabilising β-Catenin and Upregulating HK2 and Glycolysis.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- METTL3-dependent mJournal of translational medicine · 2026Article
- Exploring the role of protein homeostasis regulation in glycolysis in head and neck tumors.Human cell · 2026Review
- Osteosarcoma immunometabolism: emerging mechanisms and clinical implications.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Osteosarcoma is a primary malignancy that is difficult to treat and is prone to developing resistance to chemotherapy. As such, it is necessary to continuously explore novel therapeutic targets. Ubiquitin-specific protease 22 (USP22) is an ubiquitin-specific protease that has been demonstrated to have potent carcinogenic effects on a variety of cancers and is involved in several biological processes. Studies have demonstrated that reprogramming of glucose metabolism is a major factor in the development and progression of osteosarcoma, and that USP22 is strongly associated with the metabolism of glucose in osteosarcoma. However, it is still unknown how precisely USP22 works in osteosarcoma. To further elucidate the expression and specific molecular mechanisms of USP22 in osteosarcoma. The results of Western blot analysis and quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed that the expression of USP22 in osteosarcoma tissues was significantly higher than that in adjacent healthy tissues. In addition, the expression of USP22 promotes the proliferation of osteosarcoma cells in a glycolytic dependent manner both in vitro and in vivo, while the knockout of USP22 is the opposite. In addition, USP22 knockout reduced the protein expression of β-catenin and hexokinase 2 (HK2) in osteosarcoma cells. In addition, the regulation of HK2 expression induced by USP22 depends on β-catenin. Mechanistically, USP22 regulates HK2 by deubiquitination and stabilising the expression of β-catenin, thereby controlling glycolysis in osteosarcoma cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.